Egr-1 deficiency in bone marrow-derived cells reduces atherosclerotic lesion formation in a hyperlipidaemic mouse model

Abstract

This study demonstrates that bone marrow-derived Egr-1 promotes macrophage accumulation, atherosclerotic lesion development, and lesion complexity.

Transcription factor EGR1 directs tendon differentiation and promotes tendon repair

“…Amplification of the molecular changes in our mouse model of Achilles tendon injury is consistent with the amplified phenotypes observed in experimentally induced models for fibrosis, atherosclerosis, cardiac hypertrophy, and liver regeneration in Egr1 -/-mutant mice (44,(46)(47)(48)(49)(50)(51).…”

MicroRNA‐146 represses endothelial activation by inhibiting pro‐inflammatory pathways

“…We find that miR-146 restrains vascular inflammation by repressing the NF-kB and EGR pathways, which play important roles in atherogenesis (Albrecht et al, 2010;Gareus et al, 2008;Harja et al, 2004). Additionally, miR-146a also targets TLR4 , which is expressed in several vascular and leukocyte cell types, and has been implicated in the etiology of atherosclerosis (den Dekker et al, 2010).…”

Differential Control of Mincle-Dependent Cord Factor Recognition and Macrophage Responses by the Transcription Factors C/EBPβ and HIF1α

“…Several reports have indicated that Egr family members are induced by Dectin-1 ligands in macrophages and DCs (34,58) or neutrophils (59) in a calcineurin/NF-AT-dependent manner, which is likely also the case after Mincle stimulation. Although there are a number of reports on genes regulated by EGR family members in innate immune cells (60)(61)(62), the direct targets of EGRs in macrophages and DCs, especially in response to CLR activation, are currently unknown. We used expression of Egrs in this study primarily as a readout for early Mincle-dependent gene expression.…”